Optimal Cerebral Perfusion Pressure During Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage.
Optimal Cerebral Perfusion Pressure During Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage.
复制标题
动脉瘤性蛛网膜下腔出血后迟发性脑缺血期间的最佳脑灌注压。
DOI：
10.1097/ccm.0000000000005396
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发表时间：
2022
影响因子：
8.8
通讯作者：
Schu
中科院分区：
文献类型：
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作者：
Weiss,Miriam;Albanna,Walid;Conzen,Catharina;Megjhani,Murad;Tas,Jeanette;Seyfried,Katharina;Kastenholz,Nick;Veldeman,Michael;Schmidt,TobiasPhilip;Schulze-Steinen,Henna;Wiesmann,Martin;Clusmann,Hans;Park,Soojin;Aries,Marcel;Schu
结论：对于蛛网膜下腔出血后迟发性脑缺血治疗，推荐采用诱导性高血压，这一点最近受到了挑战，理想的压力目标缺失。一个新的概念主张一个单独的脑灌注压，脑自动调节功能最好，以确保最佳的全球灌注。我们描述了迟发性脑缺血时的最佳脑灌注压，并测试了诱导性高血压与此目标值的一致性。设计：前瞻性收集数据的回顾性分析。单位：大学医院神经重症监护室。患者：39例接受有创神经监测的蛛网膜下腔出血患者（20例迟发性脑缺血，19例无迟发性脑缺血）.干预：诱导高血压大于180 mm Hg收缩压.测量和主要结果：变点分析用于计算脑灌注压的显著变化，最佳脑灌注压，延迟性脑缺血诊断前48 h脑灌注压与最佳脑灌注压的差值。最佳脑灌注压在迟发性脑缺血发作前30小时由82.8± 12.5mmHg增加到86.3± 11.4mmHg（p< 0.05）。迟发性脑缺血前3小时，脑灌注压与最佳脑灌注压之差也出现了一个变化点（从-0.2 ±11.2 mmHg降至-7.7 ±7.6 mmHg; p< 0.05），相应的压力反应性指数增加（从0.09±0.33增至0.19±0.37; p< 0.05）。在可比较的时间范围内，迟发性脑缺血时的脑灌注压低于未发生迟发性脑缺血的患者（迟发性脑缺血时的脑灌注压为81.4±8.3 mm Hg，未发生迟发性脑缺血时的脑灌注压为90.4±10.5 mm Hg; p< 0.05）。诱导高血压导致脑灌注压高于最佳脑灌注压（+ 12.4±8.3 mm Hg; p< 0.0001）。治疗反应（迟发性脑缺血改善：诱发性高血压+[n= 15]或迟发性脑缺血进展：诱发性高血压-[n= 5]）与脑灌注压绝对值或最佳脑灌注压无关，（脑灌注压[p= 0.69];最佳脑灌注压[p= 0.97];以及脑灌注压和最佳脑灌注压的差值[p= 0.51]）。
OBJECTIVES:The recommendation of induced hypertension for delayed cerebral ischemia treatment after aneurysmal subarachnoid hemorrhage has been challenged recently and ideal pressure targets are missing. A new concept advocates an individual cerebral perfusion pressure where cerebral autoregulation functions best to ensure optimal global perfusion. We characterized optimal cerebral perfusion pressure at time of delayed cerebral ischemia and tested the conformity of induced hypertension with this target value.DESIGN:Retrospective analysis of prospectively collected data.SETTING:University hospital neurocritical care unit.PATIENTS:Thirty-nine aneurysmal subarachnoid hemorrhage patients with invasive neuromonitoring (20 with delayed cerebral ischemia, 19 without delayed cerebral ischemia).INTERVENTIONS:Induced hypertension greater than 180 mm Hg systolic blood pressure.MEASUREMENTS AND MAIN RESULTS:Changepoint analysis was used to calculate significant changes in cerebral perfusion pressure, optimal cerebral perfusion pressure, and the difference of cerebral perfusion pressure and optimal cerebral perfusion pressure 48 hours before delayed cerebral ischemia diagnosis. Optimal cerebral perfusion pressure increased 30 hours before the onset of delayed cerebral ischemia from 82.8±12.5 to 86.3±11.4 mm Hg (p< 0.05). Three hours before delayed cerebral ischemia, a changepoint was also found in the difference of cerebral perfusion pressure and optimal cerebral perfusion pressure (decrease from–0.2±11.2 to–7.7±7.6 mm Hg; p< 0.05) with a corresponding increase in pressure reactivity index (0.09±0.33 to 0.19±0.37; p< 0.05). Cerebral perfusion pressure at time of delayed cerebral ischemia was lower than in patients without delayed cerebral ischemia in a comparable time frame (cerebral perfusion pressure delayed cerebral ischemia 81.4±8.3 mm Hg, no delayed cerebral ischemia 90.4±10.5 mm Hg; p< 0.05). Inducing hypertension resulted in a cerebral perfusion pressure above optimal cerebral perfusion pressure (+ 12.4±8.3 mm Hg; p< 0.0001). Treatment response (improvement of delayed cerebral ischemia: induced hypertension+[n= 15] or progression of delayed cerebral ischemia: induced hypertension–[n= 5]) did not correlate to either absolute values of cerebral perfusion pressure or optimal cerebral perfusion pressure, nor the resulting difference (cerebral perfusion pressure [p= 0.69]; optimal cerebral perfusion pressure [p= 0.97]; and the difference of cerebral perfusion pressure and optimal cerebral perfusion pressure [p= 0.51]).CONCLUSIONS: